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miR-324-5p protects against oxidative stress-induced endothelial progenitor cell injury by targeting Mtfr1

Peier Chen1, Jianfeng Zhong1, Jianfeng Ye2

  • 1Guangdong Key Laboratory of Age-Related Cardiac and Cerebral Diseases, The Affiliated Hospital of Guangdong Medical University, Zhanjiang, Guangdong, China.

Journal of Cellular Physiology
|May 9, 2019
PubMed

Insights

MicroRNAs (miRNAs) like miR-324-5p are crucial for endothelial progenitor cell (EPC) function after heart attack. Restoring miR-324-5p levels protects EPCs from oxidative stress and injury by regulating the Mtfr1 gene.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Cellular Therapeutics

Background:

  • Endothelial progenitor cells (EPCs) are vital for vascular repair but are vulnerable to injury after acute myocardial infarction (AMI).
  • MicroRNA (miRNA) dysregulation, specifically reduced miR-324-5p in ST-segment elevation myocardial infarction (STEMI) patients, impairs EPC function.
  • Oxidative stress exacerbates EPC dysfunction, highlighting the need for protective strategies.

Purpose of the Study:

  • To investigate the role of miR-324-5p in protecting EPCs against oxidative stress-induced injury.
  • To determine if restoring miR-324-5p levels can enhance EPC function and survival.
  • To elucidate the molecular mechanism underlying miR-324-5p-mediated protection.

Main Methods:

  • Collected peripheral blood from healthy volunteers and STEMI patients to isolate EPCs.
  • Exposed EPCs to hydrogen peroxide (H2O2) and transfected them with miR-324-5p mimic.
  • Assessed EPC viability, DiI-Ac-LDL uptake, FITC-UEA-I binding, proliferation, mitochondrial function, and apoptosis pathways.
  • Utilized small RNA sequencing and Western blot to identify miR-324-5p targets, confirming Mtfr1 as a target.

Main Results:

  • STEMI patients exhibited significantly lower miR-324-5p levels in peripheral blood EPCs compared to healthy controls.
  • miR-324-5p mimic transfection improved viability, DiI-Ac-LDL uptake, FITC-UEA-I binding, and proliferation in H2O2-treated EPCs.
  • miR-324-5p suppressed mitochondrial fragmentation, enhanced membrane potential and ATP levels, and reduced apoptosis.
  • Mtfr1 was identified as a direct target gene of miR-324-5p.

Conclusions:

  • miR-324-5p plays a protective role against oxidative stress-induced injury in EPCs.
  • Restoration of miR-324-5p enhances EPC function and survival by improving mitochondrial integrity and reducing apoptosis.
  • The protective effect of miR-324-5p is mediated through the regulation of its target gene, Mtfr1.
Keywords:
EPCsMtfr1injurymiR-324-5poxidative stress

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